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Insulin resistance

SHBG, Sex hormone-binding globulin.

SHBG, Sex hormone-binding globulin.

Figure 32.1 Insulin-mediated increase in testosterone and decrease in sex hormone-binding blobulin (SHBG)

treatment of female to male transsexuals (15) and studies of the effect of testosterone on insulin sensitivity in female rats (16) have suggested that hy-perandrogenicity may also induce muscular and systemic insulin resistance. This might partly be due to a diminished insulin binding to a contracted bed of capillary endothelium, and subsequent diminished blood flow and insufficient delivery of insulin to its site of action on the muscle cell (16). Postreceptor perturbations may also be involved.

Whatever the cause-effect sequence it is clear that hyperandrogenicity in women is closely associated with insulin resistance. Furthermore, this is not a rare condition and it is estimated that about 20% of middle-aged women of a non-selected population may be hyperandrogenic with SHBG values in the lower range (17). The increased risk of disease therefore is a problem of considerable quantitative importance.

Figure 32.2 The effects of testosterone on visceral adipose tissue (AT). Lipid uptake is inhibited and mobilization is stimulated with an increased release of free fatty acids (FFA)

suppression by diazoxide (19), are in accordance with the concept that insulin inhibits SHBG synthesis and stimulates testosterone production.

However, since obese men usually have a lowered baseline testosterone concentration these findings do not fully explain the cause-effect sequence. Therefore, probably other mechanisms are also involved. Recently, Vermeulen (20) suggested that hy-pogonadism in obese men has a central, hy-pothalamo-pituitary origin since a group of obese men had decreased luteinizing hormone (LH) pulse amplitude and decreased free testosterone concentration, but a normal response of the Leydig cells to chorion gonadotrophin stimulation.

Consequently, it may be hypothesized that the hypogonadism in obese men may be at least partly of neuroendocrine origin, but other factors, such as the insulin-mediated suppression of SHBG synthesis, play an additional role.

Hypoandrogenicity and Insulin Resistance in Men

In men, data on the direction of causality between testosterone and insulin resistance are more scarce. Previous findings of a positive correlation between insulin sensitivity and SHBG levels in men with type 2 diabetes (18), and increased SHBG concentration and reduced testosterone levels after insulin

Testosterone and Adipose Tissue

Previous works (21,22) on lipid transport to and mobilization from adipose tissue measured in vivo in men have shown that lipid uptake and mobilization are higher in intra-abdominal adipose tissue than in subcutaneous (s.c.) ones. After testosterone treatment, lipid uptake is markedly inhibited, apparently more in s.c. abdominal fat than in s.c. femoral fat and particularly in intra-abdominal adi-

TREATMENT: HORMONES Table 32.2 Effects of testosterone treatment in men


Duration of treatment

Body composition

Metabolic variables

8 months

6 weeks

9 months 3 months

J, Visceral fat

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